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231223s2008 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2008.03.460
|2 doi
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|a pubmed24n0597.xml
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|a (DE-627)NLM17918878X
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|a (NLM)18439876
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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1 |
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|a Morrison, Paul T
|e verfasserin
|4 aut
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|a Chemokine-receptor upregulation and disease severity in respiratory syncytial virus infection
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|c 2008
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
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|2 rdamedia
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|a ƒa Online-Ressource
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|a Date Completed 15.07.2008
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|a Date Revised 20.06.2008
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Respiratory Syncytial Virus (RSV) infection is an important cause of severe infant bronchiolitis, partly due to lower airway inflammation orchestrated by virus-induced chemokine secretion. Chemokine receptors may therefore be therapeutic targets. We investigated RSV-induced chemokine receptor (CCR) 1, 2 and 5 surface expressions in a cellular model and in infants. RSV infection increased human monocytic CCR1, 2 and 5 expression, as assessed by FACS, via replication-dependent mechanisms. CCR1 and CCR5 levels peaked at 36 h and CCR2 levels at 48 h. Monocytes from infants with RSV-bronchiolitis significantly increased CCR1 expression after ex vivo RSV infection compared to controls. Expression of CCR5 also increased, and correlated with CCR1 expression (r=0.78, p<0.0001). CCR1 upregulation correlated with disease severity markers. Monocyte CCR1 receptors were functionally active as stimulation resulted in calcium influx. CCR1/5 blocking strategies may be useful in decreasing cellular inflammation in RSV infection
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a CCR1 protein, human
|2 NLM
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|a CCR2 protein, human
|2 NLM
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|a Receptors, CCR1
|2 NLM
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|a Receptors, CCR2
|2 NLM
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|a Receptors, CCR5
|2 NLM
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1 |
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|a Sharland, Mike
|e verfasserin
|4 aut
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1 |
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|a Thomas, Lynette H
|e verfasserin
|4 aut
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700 |
1 |
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|a Manna, Soumendu
|e verfasserin
|4 aut
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700 |
1 |
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|a Handforth, Jenny
|e verfasserin
|4 aut
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1 |
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|a Tibby, Shane
|e verfasserin
|4 aut
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1 |
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|a Friedland, Jon S
|e verfasserin
|4 aut
|
773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 128(2008), 1 vom: 01. Juli, Seite 85-93
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
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|g volume:128
|g year:2008
|g number:1
|g day:01
|g month:07
|g pages:85-93
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|u http://dx.doi.org/10.1016/j.clim.2008.03.460
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|d 128
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